Cardiac Control: The Cardiac Center in the medulla.

Outputs:

The cardioacceleratory center sends impulses through the sympathetic nervous system in the cardiac nerves. These fibers innervate the SA node and AV node and the ventricular myocardium. Effects on the SA and AV nodes are an increase in depolarization rate by reducing the resting membrane polarization. Effect on the myocardium is to increase contractility thus increasing force and therefore volume of contraction. Sympathetic stimulation increases both rate and volume of the heart.

The cardioinhibitory center sends impulses through the parasympathetic division, the vagus nerve, to the SA and AV nodes, but only sparingly to the atrial myocardium, and not at all to ventricular myocardium. Its effect is to slow the rate of depolarization by increasing the resting potential, i.e. hyperpolarization.

The parasympathetic division controls the heart at rest, keeping its rhythm slow and regular. This is referred to as normal vagal tone. Parasympathetic effects are inhibited and the sympathetic division exerts its effects during stress, i.e. exercise, emotions, "fight or flight" response, and temperature.

Inputs to the Cardiac Center:

Baroreceptors in the aortic and carotid sinuses. The baroreceptor reflex is responsible for the moment to moment maintenance of normal blood pressure.

Higher brain (hypothalamus): stimulates the center in response to exercise, emotions, "fight or flight", temperature.

Intrinsic Controls of the Heart:

Right Heart Reflex - Pressoreceptors (stretch receptors) in the right atrium respond to stretch due to increased venous return. The reflex acts through a short neural circuit to stimulate the sympathetic nervous system resulting in increased rate and force of contraction. This regulates output to input

The Frank-Starling Law - (Starling's Law of the Heart) - Like skeletal muscle the myocardium has a length tension curve which results in an optimum level of stretch producing the maximum force of contraction. A healthy heart normally operates at a stretch less than this optimum level and when exercise causes increased venous return and increased stretch of the myocardium, the result is increased force of contraction to automatically pump the increased volume out of the heart. I.e. the heart automatically compensates its output to its input.

An important relationship in cardiac output is this one:

Blood Flow =  D Pressure / Resistance to Blood Flow      

The Nerve Impulse

When a nerve is stimulated the resting potential changes. Examples of such stimuli are pressure, electricity, chemicals, etc. Different neurons are sensitive to different stimuli(although most can register pain). The stimulus causes sodium ion channels to open. The rapid change in polarity that moves along the nerve fiber is called the "action potential." In order for an action potential to occur, it must reach threshold. If threshold does not occur, then no action potential can occur. This moving change in polarity has several stages:

Depolarization

The upswing is caused when positively charged sodium ions (Na+) suddenly rush through open sodium gates into a nerve cell. The membrane potential of the stimulated cell undergoes a localized change from -55 millivolts to 0 in a limited area. As additional sodium rushes in, the membrane potential actually reverses its polarity so that the outside of the membrane is negative relative to the inside. During this change of polarity the membrane actually develops a positive value for a moment(+30 millivolts). The change in voltage stimulates the opening of additional sodium channels (called a voltage-gated ion channel). This is an example of a positive feedback loop.

Repolarization

The downswing is caused by the closing of sodium ion channels and the opening of potassium ion channels. Release of positively charged potassium ions (K+) from the nerve cell when potassium gates open. Again, these are opened in response to the positive voltage--they are voltage gated. This expulsion acts to restore the localized negative membrane potential of the cell (about -65 or -70 mV is typical for nerves).

Hyperpolarization

When the potassium ions are below resting potential (-90 mV). Since the cell is hyper polarized, it goes to a refractory phrase.

Refractory phase

The refractory period is a short period of time after the depolarization stage. Shortly after the sodium gates open, they close and go into an inactive conformation. The sodium gates cannot be opened again until the membrane is repolarized to its normal resting potential. The sodium-potassium pump returns sodium ions to the outside and potassium ions to the inside. During the refractory phase this particular area of the nerve cell membrane cannot be depolarized. This refractory area explains why action potentials can only move forward from the point of stimulation.

Factors that affect sensitivity and speed

Sensitivity

Increased permeability of the sodium channel occurs when there is a deficit of calcium ions. When there is a deficit of calcium ions (Ca+2) in the interstitial fluid, the sodium channels are activated (opened) by very little increase of the membrane potential above the normal resting level. The nerve fiber can therefore fire off action potentials spontaneously, resulting in tetany. This could be caused by the lack of hormone from parathyroid glands. It could also be caused by hyperventilation, which leads to a higher pH, which causes calcium to bind and become unavailable.

Speed of Conduction

This area of depolarization/repolarization/recovery moves along a nerve fiber like a very fast wave. In myelinated fibers, conduction is hundreds of times faster because the action potential only occurs at the nodes of Ranvier (pictured below in 'types of neurons') by jumping from node to node. This is called "saltatory" conduction. Damage to the myelin sheath by the disease can cause severe impairment of nerve cell function. Some poisons and drugs interfere with nerve impulses by blocking sodium channels in nerves. See discussion on drug at the end of this outline.

The Nervous System Has Peripheral and Central Units

• The central nervous system (CNS) is the brain and spinal column
• The peripheral nervous system (PNS) consists of nerves outside of the CNS
• There are 31 pairs of spinal nerves (mixed motor & sensory)
• There are 12 pairs of cranial nerves (some are pure sensory, but most are mixed)

The pattern of innervation plotted on the skin is called a dermatome

The Nervous System Has Peripheral and Central Units

• The central nervous system (CNS) is the brain and spinal column
• The peripheral nervous system (PNS) consists of nerves outside of the CNS
• There are 31 pairs of spinal nerves (mixed motor & sensory)
• There are 12 pairs of cranial nerves (some are pure sensory, but most are mixed)

The pattern of innervation plotted on the skin is called a dermatome

Bile - produced in the liver and stored in the gallbladder, released in response to CCK . Bile salts (salts of cholic acid) act to emulsify fats, i.e. to split them so that they can mix with water and be acted on by lipase.

Pancreatic juice: Lipase - splits fats into glycerol and fatty acids. Trypsin, and chymotrypsin - protease enzymes which break polypeptides into dipeptides. Carboxypeptidase - splits dipeptide into amino acids. Bicarbonate - neutralizes acid. Amylase - splits polysaccharides into shorter chains and disaccharides.

Intestinal enzymes (brush border enzymes): Aminopeptidase and carboxypeptidase - split dipeptides into amino acids. Sucrase, lactase, maltase - break disaccharides into monosaccharides. Enterokinase - activates trypsinogen to produce trypsin. Trypsin then activates the precursors of chymotrypsin and carboxypeptidase. Other carbohydrases: dextrinase and glucoamylase. These are of minor importance.

Blood Groups

Blood groups are created by molecules present on the surface of red blood cells (and often on other cells as well).

The ABO Blood Groups

The ABO blood groups are the most important in assuring safe blood transfusions.

When red blood cells carrying one or both antigens are exposed to the corresponding antibodies, they agglutinate; that is, clump together. People usually have antibodies against those red cell antigens that they lack.

The critical principle to be followed is that transfused blood must not contain red cells that the recipient's antibodies can clump. Although theoretically it is possible to transfuse group O blood into any recipient, the antibodies in the donated plasma can damage the recipient's red cells. Thus all transfusions should be done with exactly-matched blood.

The Rh System

Rh antigens are transmembrane proteins with loops exposed at the surface of red blood cells. They appear to be used for the transport of carbon dioxide and/or ammonia across the plasma membrane. They are named for the rhesus monkey in which they were first discovered.

There are a number of Rh antigens. Red cells that are "Rh positive" express the one designated D. About 15% of the population have no RhD antigens and thus are "Rh negative".

The major importance of the Rh system for human health is to avoid the danger of RhD incompatibility between mother and fetus.

During birth, there is often a leakage of the baby's red blood cells into the mother's circulation. If the baby is Rh positive (having inherited the trait from its father) and the mother Rh-negative, these red cells will cause her to develop antibodies against the RhD antigen. The antibodies, usually of the IgG class, do not cause any problems for that child, but can cross the placenta and attack the red cells of a subsequent Rh⁺ fetus. This destroys the red cells producing anemia and jaundice. The disease, called erythroblastosis fetalis or hemolytic disease of the newborn, may be so severe as to kill the fetus or even the newborn infant. It is an example of an antibody-mediated cytotoxicity disorder.

Although certain other red cell antigens (in addition to Rh) sometimes cause problems for a fetus, an ABO incompatibility does not. Rh incompatibility so dangerous when ABO incompatibility is not

It turns out that most anti-A or anti-B antibodies are of the IgM class and these do not cross the placenta. In fact, an Rh⁻/type O mother carrying an Rh⁺/type A, B, or AB fetus is resistant to sensitization to the Rh antigen. Presumably her anti-A and anti-B antibodies destroy any fetal cells that enter her blood before they can elicit anti-Rh antibodies in her.

This phenomenon has led to an extremely effective preventive measure to avoid Rh sensitization. Shortly after each birth of an Rh⁺ baby, the mother is given an injection of anti-Rh antibodies. The preparation is called Rh immune globulin (RhIG) or Rhogam. These passively acquired antibodies destroy any fetal cells that got into her circulation before they can elicit an active immune response in her.

Rh immune globulin came into common use in the United States in 1968, and within a decade the incidence of Rh hemolytic disease became very low.

Concentration versus diluting urine 

Kidney is a major route for eliminating fluid from the body to accomplish water balance. Urine excretion is the last step in urine formation. Everyday both kidneys excrete about 1.5 liters of urine.
Depending on the hydrated status of the body, kidney either excretes concentrated urine ( if the plasma is hypertonic like in dehydrated status ) or diluted urine ( if the plasma is hypotonic) .
This occurs thankful to what is known as countercurrent multiplying system, which functions thankfully to establishing large vertical osmotic gradient .
To understand this system, lets review the following facts:
1. Descending limb of loop of Henle is avidly permeable to water.
2. Ascending limb of loop of Henly is permeable to electrolytes , but impermeable to water. So fluid will not folow electrolytes by osmosis.and thus Ascending limb creates hypertonic interstitium that will attract water from descending limb.
Pumping of electrolytes
3. So: There is a countercurrent flow produced by the close proximity of the two limbs.                   
                                                   
Juxtamedullary nephrons have long loop of Henle that dips deep in the medulla , so the counter-current system is more obvious and the medullary interstitium is always hypertonic . In addition, peritubular capillaries in the medulla are straigh ( vasa recta) in which flow is rapid and rapidly reabsorb water maintaining hypertonic medullary interstitium.

In distal tubules water is diluted. If plasma is hypertonic, this will lead to release of ADH by hypothalamus, which will cause reabsorption of water in collecting tubules and thus excrete concentrated urine.

If plasma is hypotonic ADH will be inhibited and the diluted urine in distal  tubules will be excreted as diluted urine.

Urea  contributes to concentrating and diluting of urine as follows:

Urea is totally filtered and then 50% of filtrated urea will be reabsorbed to the interstitium, this will increase the osmolarity of medullary interstitium ( becomes hypertonic ). Those 50% will be secreted in ascending limb of loop of Henle back to tubular fluid to maintain osmolarity of tubular fluid. 55% of urea in distal nephron will be reabsorbed in collecting ducts back to the interstitium ( under the effect of ADH too) . This urea cycle additionally maintain hypertonic interstitium.